Functional dyspepsia and gastroparesis are common gastrointestinal disorders, sharing similar symptoms such as early satiety, bothersome postprandial fullness, epigastric pain or burning, bloating, belching, nausea and vomiting. Gastroparesis is characterized by delayed gastric emptying, and functional dyspepsia is associated with similar but more diverse pathophysiological changes including impaired gastric accommodation, gastric/duodenal hypersensitivity, low-grade inflammation, and increased mucosal permeability. The traditional non-targeted therapies failed to be effective for the majority of patients, largely due to the diverse pathophysiological changes and the unclear mechanisms underlying them. It is becoming clear that new therapeutic options, targeting specific pathophysiological and molecular changes based on individuals, are needed for the treatment of these disorders.
It is well acknowledged that the disruption of the bidirectional communication in the gut-brain axis contributes to the development of functional dyspepsia and gastroparesis. However, our current knowledge of the molecular mechanisms along the gut-brain axis in these disorders is still limited. Understanding the complex mechanisms will have the potential to yield novel new targets for the treatment of these disorders. This process will increasingly involve laboratory animal models, besides traditional clinical research.
This collection will explore the mechanisms in the gut-brain axis in functional dyspepsia and gastroparesis. Areas of interest include, but not limited to the following aspects of these disorders:
• Alteration in the nervous system including the brain, parasympathetic nerves, sympathetic nerves and gastrointestinal enteric nerves
• Alteration in gastrointestinal mechanisms including the immune system, gastrointestinal microbiota and dietary factors
• Clinical implications of the existing mechanisms in the gut-brain axis
• Laboratory animal models
We welcome original articles, methods and reviews, and both clinical and pre-clinical studies.
Functional dyspepsia and gastroparesis are common gastrointestinal disorders, sharing similar symptoms such as early satiety, bothersome postprandial fullness, epigastric pain or burning, bloating, belching, nausea and vomiting. Gastroparesis is characterized by delayed gastric emptying, and functional dyspepsia is associated with similar but more diverse pathophysiological changes including impaired gastric accommodation, gastric/duodenal hypersensitivity, low-grade inflammation, and increased mucosal permeability. The traditional non-targeted therapies failed to be effective for the majority of patients, largely due to the diverse pathophysiological changes and the unclear mechanisms underlying them. It is becoming clear that new therapeutic options, targeting specific pathophysiological and molecular changes based on individuals, are needed for the treatment of these disorders.
It is well acknowledged that the disruption of the bidirectional communication in the gut-brain axis contributes to the development of functional dyspepsia and gastroparesis. However, our current knowledge of the molecular mechanisms along the gut-brain axis in these disorders is still limited. Understanding the complex mechanisms will have the potential to yield novel new targets for the treatment of these disorders. This process will increasingly involve laboratory animal models, besides traditional clinical research.
This collection will explore the mechanisms in the gut-brain axis in functional dyspepsia and gastroparesis. Areas of interest include, but not limited to the following aspects of these disorders:
• Alteration in the nervous system including the brain, parasympathetic nerves, sympathetic nerves and gastrointestinal enteric nerves
• Alteration in gastrointestinal mechanisms including the immune system, gastrointestinal microbiota and dietary factors
• Clinical implications of the existing mechanisms in the gut-brain axis
• Laboratory animal models
We welcome original articles, methods and reviews, and both clinical and pre-clinical studies.
